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Emotional contagion refers to the mechanism of aligning with conspecifics' emotional states and is thought to be highly beneficial in social group living. While emotional contagion is well studied in humans, most studies in nonhuman animals fail to clearly distinguish between behavioural and emotional contagion. Furthermore, evidence for positive emotional contagion in nonhuman animals is almost entirely restricted to the context of play. In the present study, we aimed at adding observational evidence of contagion in a positive context, while separating aspects of behavioural and emotional contagion. In a group of nonbreeder common ravens, Corvus corax , we investigated whether witnessing conspecifics in positive social interaction, namely allopreening, would influence a bystander's behavioural and, possibly, emotional state. We recorded behavioural expressions of bystanders in postpreening observation phases and compared them to those in matched-control observation phases. We found effects of witnessing others' allopreening on the bystanders' subsequent affiliative interactions but not on their self-directed behaviours (e.g. autopreening) or agonistic interactions. Specifically, bystanders were more likely to engage in allopreening themselves in the postpreening observation phase than in the matched-control observation phase, which could be explained via behavioural and emotional contagion; however, bystanders also showed elevated levels of nonpreening affiliative interactions and spent more time close to conspecifics after observing others allopreening, which hints towards a more general effect on the bystanders' emotional states. Whether these nonpreening affiliative interactions are indeed an indication of emotional contagion needs to be tested in further studies that measure, and manipulate, emotional states.

Perceiving, evaluating and reacting towards conspecifics' emotional states are important challenges of social group living. Emotional contagion describes an alignment of emotional states between individuals and is widely believed to be based on behavioral synchronization, i.e., behavioral contagion. As basic empathy-like processes, the occurrence of both forms of contagion seems to underlie early ontogenetic trajectories in humans and non-human species. In the present study, we assessed play as a context for studying the development of emotional contagion and its interlink with behavioral contagion in ten juvenile common ravens. Ravens are exceptional players that engage in all three forms of play: object, locomotion and social play. To assess potential ontogenetic patterns of both behavioral and emotional contagion, we tested juvenile ravens at two different periods of early development, at three- and six-month post-hatching. We elicited object play in one or several ravens (demonstrators) in a standardized experimental environment, using a playground setup. At both test ages, we found evidence for emotional contagion as observer ravens showed an increase of locomotion and social play after we provided the demonstrator(s) with the playground setup, but no significant changes in the amount of object play. Hence, observers did not copy motor patterns from demonstrator(s) but engaged in other forms of play. Our findings speak for a transfer of a general mood state in the context of play in ravens as young as 3 months and against behavioral mimicry as a precondition for emotional contagion.

Learning allows animals to respond to changes in their environment within their lifespan. However, many responses to the environment are innate, and need not be learned. Depending on the level of cognitive flexibility an animal shows, such responses can either be modified by learning or not. Many ants deposit pheromone trails to resources, and innately follow such trails. Here, we investigated cognitive flexibility in the ant Lasius niger by asking whether ants can overcome their innate tendency and learn to avoid conspecific pheromone trails when these predict a negative stimulus. Ants were allowed to repeatedly visit a Y-maze, one arm of which was marked with a strong but realistic pheromone trail and led to a punishment (electric shock and/or quinine solution), and the other arm of which was unmarked and led to a 1 mol l-1 sucrose reward. After ca. 10 trials, ants stopped relying on the pheromone trail, but even after 25 exposures they failed to improve beyond chance levels. However, the ants did not choose randomly: rather, most ants began to favour just one side of the Y-maze, a strategy which resulted in more efficient food retrieval over time, when compared with the first visits. Even when trained in a go/no-go paradigm which precludes side bias development, ants failed to learn to avoid a pheromone trail. These results show rapid learning flexibility towards an innate social signal, but also demonstrate a rarely seen hard limit to this flexibility., Competing Interests: Competing interests The authors declare no competing or financial interests., (© 2021. Published by The Company of Biologists Ltd.)

The exosome, a large multisubunit complex with exoribonucleic activity, emerges as the central 3' RNA degradation and processing factor in eukaryotes and archaea. But how are the many RNA substrates of the exosome degraded in a processive, yet controlled manner? Recent functional and structural progress shows that the exosome is a macromolecular cage, where the nuclease active sites are situated in a central processing chamber. A narrow entry pore controls access to the active sites in the processing chamber and prevents uncontrolled RNA decay. The emerging mechanism of exosome function suggests a strikingly parallel architectural concept to protein degradation by proteasomes.

In acute myeloid leukemia (AML), two clusters of activating mutations are known in the FMS-like tyrosine kinase-3 (FLT3) gene: FLT3-internal tandem duplications (FLT3-ITDs) in the juxtamembrane (JM) domain in 20% to 25% of patients, and FLT3 point mutations in the tyrosine-kinase domain (FLT3-TKD) in 7% to 10% of patients, respectively. Here, we have characterized a new class of activating point mutations (PMs) that cluster in a 16-amino acid stretch of the juxtamembrane domain of FLT3 (FLT3-JM-PMs). Expression of 4 FLT3-JM-PMs in interleukin-3 (IL-3)-dependent Ba/F3 cells led to factor-independent growth, hyperresponsiveness to FLT3 ligand, and resistance to apoptotic cell death. FLT3-JM-PM receptors were autophosphorylated and showed a higher constitutive dimerization rate compared with the FLT3-wild-type (WT) receptor. As a molecular mechanism, we could show activation of STAT5 and up-regulation of Bcl-x(L) by all FLT3-JM-PMs. The FLT3 inhibitor PKC412 abrogated the factor-independent growth of FLT3-JM-PM-expressing cells. Compared with FLT3-ITD and FLT3-TKD mutants, the FLT3-JM-PMs showed a weaker transforming potential related to lower autophosphorylation of the receptor and its downstream target STAT5. Mapping of the FLT3-JM-PMs on the crystal structure of FLT3 showed that these mutations reduce the stability of the autoinhibitory JM domain, and provides a structural basis for the transforming capacity of this new class of gain-of-function mutations of FLT3.